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ICS/GP/ILA > ILA > Flashcards

ILA Flashcards

1
Q

What are the 3 layers of the normal arterial vessel wall?

A
  1. tunica intima - simple squamous with connective basement membrane
  2. tunica media - middle layer of smooth muscle (often thickest)
  3. tunica adventitia - outermost made of elastin and collagen
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2
Q

What is a plaque composed of?

A
  • necrotic and lipid core
  • inflammatory cells (macrophages & T lymph)
  • fibrous cap made from smooth muscle
  • cellular lipids and debris
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3
Q

What leads to plaque formation?

A

Chronic or episodic exposure of arterial wall so plaques often form at branching sites

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4
Q

Formation of Plaques?

A
  1. damage to endothelial cells cause them to become more permeable. Lipids and inflammatory cells enter and form plaques.
    > high levels of LDLs oxidise
  2. macrophages phagocytose LDLs and release lipids as foam cells
    > support migration of smooth muscle into
    intima and increased collagen synthesis
    > die and leak lipids –> fatty streak
  3. foam cells release growth factors so smooth muscle proliferates into fibrous cap
  4. new vessels form (vasa vasorum) within plaque, expand, and haemorrhage causing plaque expansion
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5
Q

What are modifiable risk factors of atherosclerosis?

A
  • smoking
  • obesity
  • hypertension
  • sedentary lifestlye
  • type 2 diabetes
  • high cholesteral
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6
Q

What are some non-modifiable risk factors for atherosclerosis?

A
  • age
  • male gender
  • family history
  • race
  • type 1 diabetes
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7
Q

Why does smoking cause atherosclerosis?

A

Damages endothelial cells due to free radicals, nicotine, and CO

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8
Q

Why does high cholesterol cause AS?

A

Increase in LDLs means more can oxidise and get stuck

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9
Q

Why does hypertension cause AS?

A

shearing force causes direct damage to endothelial cells

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10
Q

What race/ethnicity is AS more common in?

A

South Asian, African, Afro-Caribbean descent

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11
Q

Why is poorly damaged diabetes a risk factor for AS?

A

superoxide anions and glycosylation products cause high glucose levels in blood and more LDL oxidation. Also, loss of NO so less vasodilation and more platelet aggregation

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12
Q

What primary preventative measures for AS?

A
  • exercise to redistribute LDLs
  • more balanced diet to reduce weight
  • reduce/stop smoking
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13
Q

What secondary preventatives for AS?

A
  • statins for cholesterol
  • antihypertensives
  • diabetes control
  • social prescribing
  • dual antiplatelet therapy
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14
Q

Define anaphylaxis.

A

An acute allergic reaction to an antigen, to which the body has become hypersensitive. Severe, life-threatening, generalised, or systemic.

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15
Q

What is the criteria that needs to be met to classify a reaction as anaphylaxis?

A
  1. sudden onset and rapid progression of symptoms
  2. life threatening airway/breathing/circulation problems associated with skin and mucosal changes
  3. occurs within mins and can last a few hours
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16
Q

What are anaphylactoids?

A

trigger agent acts on mast cell rather than IgE and presents as idiopathic

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17
Q

What are some examples of trigger agents for anaphylaxis?

A

Food - peanuts, tree nuts, shellfish, eggs, lactose, gluten
Drugs - antibiotics, opioids, NSAIDs, anaesthetics
Venom - bee and wasp stings
Hospital - latex, plasters, radiocontrast injections

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18
Q

What type of hypersensitvity reaction is anaphylaxis?

A

Type 1 so involves IgE antibodies

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19
Q

What do IgE receptors bind to?

A

mast cells and basophils - antibodies primed so can react quickly when next come into contact with antigen

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20
Q

How is histamine released during anaphylaxis?

A

cross-linking causes rapid cellular degranulation and liberation of chemical mediators (histamine, protease, proteoglycans, dhemotactic)

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21
Q

What are the physiological responses of anaphylaxis?

A
  • smooth muscle spasm in resp and GI tracts
  • vasodilation/increased vascular permeability
  • increased mucous secretion and bronchial smooth muscle tone
  • decreased vascular tone, capillary leakage, hypotension, arrhythmia, syncope, shock
  • histamine makes blood vessels/bronchioles leaky –> causes wheezing and shock due to large fluid loss from circulation
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22
Q

What is rapid assessment of anaphylaxis?

A

Airway, Breathing, Circulation, Disibility, Exposure

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23
Q

What guidelines for treatment of anaphylaxis?

A
  1. remove cause
  2. adrenaline into anterolateral middle thigh
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24
Q

What are the recommended dosages of adrenaline?

A

adults = 500ug, children < 12 = 300ug, children < 6 = 150ug

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25
Q

How does adrenaline relieve anaphylaxis?

A
  • stimulates beta 1 receptors so HR and contraction increase
  • stimulates beta 2 receptors so more bronchodilation
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26
Q

What can you do to alleviate anaphylaxis when more help is available?

A
  • establish airway and high flow O2
  • IV fluids
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27
Q

Why might a second dose of adrenaline be needed?

A

short half life of 2-3 mins

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28
Q

What is the confirmatory blood test for anaphylaxis?

A

mast cell tryptase - elevated up to 6 hours after

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29
Q

What are risk factors for anaphylaxis?

A
  • those with other allergies
  • older age, women > men
  • new allergens and pollutants
  • increase in antibiotics
  • more caesarean births
  • more processed diets
    These all mean less exposire to healthy gut microbiome and weaker immune system.
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30
Q

What two characteristics should drugs have to be able to act quickly, specifically analgesics?

A
  1. Low protein binding - protein binding lowers free concentration so if low then high plasma concentration
  2. High lipid solubility - allows drug to cross BBB through astrocytes
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31
Q

What is the difference between volatile and IV anaesthetic?

A

Gas can be kept at a good level whereas IV isn’t as sustainable - it builds up and happens more quickly.

32
Q

What is an agonist?

A

A compound that binds to a receptor and activates it to produce a response

33
Q

What is an example of an agonist?

A

Adrenaline is agonist of B-adrenoreceptors because it increases heart rate

34
Q

What is a full agonist?

A

High efficacy so produces full repsonse whilst occupying low proportion of receptors

35
Q

What is a partial agonist?

A

Sub-maximal activation even when all receptors occupied

36
Q

What is an inverse agonist?

A

Produces opposite effect to agonist but binds to same site on receptor

37
Q

What is an antagonist?

A

Compound that prevents agonist from binding to a receptor and reduces effect of agonist

38
Q

Example of antagonist?

A

Propranolol prevents tachycardia

39
Q

What is a competitive antagonist and give example.

A
  • reversible and surmountable
  • binds to same site
  • increasing agonist undoes action
    Eg. naloxone for opioid receptor
40
Q

What is a non-competitive antagonist and give example.

A
  • irreversible and insurmountable
  • binds to allosteric site
    Eg. ketamine and NMDA-glutamate receptor.
41
Q

Example of enzyme drug target?

A

ACE Inhibitors

42
Q

Example of transporter drug target?

A

PPIs

43
Q

Example of ion channel drug targets?

A

Amlodipine CCB

44
Q

Definition of bioavailability.

A

How much a drug is available over a given time in systemic circulation.
IV is 100%, oral is always lower

45
Q

What is first pass metabolism?

A

Metabolism of a drug into inactive compounds in the liver, after enteric absorption but before it reaches the systemic circulation

46
Q

Pathway of drug to liver?

A

intestinal lumen –> intestinal wall –> membrane transporters –> liver

47
Q

Is dose of morphine higher when given orally or IV?

A

Orally

48
Q

Why are lower doses/longer intervals of morphine used for patients with renal impairement?

A

Morphine matabolised to morphine 6 glucuronide which is more potent and renally excreted.

If renally impaired, this could build up and cause respiratory depression due to high opioid sensitivity and reduced renal clearance.

49
Q

Why does opioid excess affect lungs?

A

Opioids activate receptors on neurones with respiratory centres.

50
Q

Difference in presentation between arterial and venous thrombosis: pulse?

A

A: dimished or absent pulse
V: pulse is present

51
Q

Difference in presentation between arterial and venous thrombosis: pain?

A

A: pain is intermittent claudication
V: pain is aching and cramping with oedema

52
Q

Difference in presentation between arterial and venous thrombosis: skin pigmentation?

A

A: skin dependent rubor
V: pigmentation in gaiter area (medial and lateral malleolus)

53
Q

Difference in presentation between arterial and venous thrombosis: nails?

A

A: thickened and ridged
V: N/A

54
Q

What are the 6Ps of arterial thrombosis?

A

Pulselessness, pain, pallor, paralysis, perishingly cold, paraesthesia

55
Q

Difference in presentation between arterial and venous thrombosis: clot colour?

A

A: white
V: red

56
Q

What blood test is done to confirm diagnosis of DVT?

A

D-Dimer test - detects pieces of blood clot that have been broken down

56
Q

Why is the D-dimer test sensitive but not specific?

A

Sensitive because high percentage of positive results, easily picks up raised D-dimers. Not specific because other things can increase it such as DIC, infection, pregnancy, malignancy.

56
Q

What drugs are used in the treatment of a DVT?

A

Heparin and warfarin

57
Q

How does warfarin work?

A

Exhibits anticoag effects via extrinsic and intrinsic pathways. limits synthesis of vit K dependent clotting factors (10,9,7,2) by inhibitng vit k reductase complex

58
Q

How does heparin work?

A

catalyst for antithrombin III which inactivates proteases in coagulation cascade by producing confirmational change

59
Q

What is the biggest complication of a DVT?

A

PE

60
Q

What are some risk factors for Virchow’s triad?

A
  • increase in age –> increases viscocity
  • long haul flights –> increases stasis so flow is not laminar
  • hypertension –> shearing forces on endothelial cells
  • smoking –> damages vessel walls due to free radicals, nicotine, and CO
  • overweight –> increases chances of plaque formation
61
Q

What is the diagnostic criteria for an AKI?

A
  1. rise in creatinine > 25 umol/l in 48 hrs
  2. rise in creatinine > 50% in 7 days
  3. urine output < 0.5 ml/kg/hr for > 6 hours
62
Q

What are the three major classes of AKI?

A
  1. pre-renal
  2. intrinsic/renal
  3. post renal
63
Q

What are examples for each of the classifications of an AKI?

A
  1. dehydration, hypotension, heart failure
  2. glomerulonephritis, interstitial nephritis, acute tubular necrosis
  3. kidney stones, abdo/prostate cancers, ureter/urethral strictures
64
Q

What is the main complication of AKI?

A

hyperkalaemia

65
Q

What changes does hyperkalaemia show on ECG?

A
  • Tall T waves
  • flattened p waves
  • prolonged PR interval
  • ST depression
66
Q

What drugs are contraindicated in an AKI? (DAMN)

A

Diuretics
ACE Inhibitors
Metformin
NSAIDs

67
Q

Definition of a stroke?

A

Acute neurological deficit lasting more than 24hrs and caused by cerebrovascular aetiology

68
Q

What are the two main types of stroke?

A

Ischaemic and Haemorrhagic

69
Q

What is the definition of a transient ischaemic attack (TIA)?

A

Transient episode of neurolgical dysfunction caused by ischaemia, without acute infarction. Effects will completely resolve within 24hrs

70
Q

What is the definition of amaurosis fugax?

A

Painless and transient visual disturbance/loss of vision due to atherosclerosis/thromboembolism in internal carotid or ophthalmic arteries.

71
Q

How does AF increase the risk of stroke?

A

Fibrillation causes stasis and pooling of blood, increasing likelihood of clot formation in the heart - and therefore embolism to the brain

72
Q

Are stroke symptoms ipsilateral or contralateral to area of brain affected?

A

Contralateral to area of ischaemia because motor and sensory nerve fibres decussate in either the spinal cord or brainstem.

73
Q

What is Cushing’s reflex?

A

Response to acute increase in ICP - resulting in hypertension, bradycardia, and erratic breathing

74
Q

What is the pathophysiological process of Cushing’s refflex?

A
  1. Ischaemia increases until ICP exceeds that of arterial BP in brain, causing it to compress
  2. Alpha 1 adrenergic receptors cause arterial smooth muscle will vasoconstrict (sympathetic) in order to increase the blood pressure and reperfuse the brain –> hypertension
  3. This causes baroreceptors in the aortic arch to simultaneously reduce the blood pressure (parasympathetic) –> bradycardia and stomach ulcers
  4. The HTN then presses on resp. centres in brain stem –> irregular breathing
75
Q

Why is Cushing’s reflex a bad sign?

A

Suggests brain herniation and death is imminent

ICS/GP/ILA (9 decks)

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